The ionic mechanisms involved in the generation of several types of postsynaptic potentials were investigated in the sympathetic ganglia of bullfrogs, by intracellular and sucrose gap recording techniques. The fast EPSP has a marked decrease in membrane resistance at its peak and has a reversal potential at -16 mV. These data, together with ion change experiments, indicate that the fast EPSP is generated by an increased membrane conductance to both sodium and potassium ions. In contrast to this increased conductance mechanism, the slow postsynaptic potentials (the slow EPSP and the slow IPSP)are generated by different membrane mechanisms. Membrane resistance is increased during the slow EPSP, and membrane polarization shows that the slow EPSP reverses near the potassium equilibrium potential. We propose that the slow EPSP, in contrast to classical fast EPSPs, is generated by an inactivation of resting potassium conductance. The slow IPSP in these neurons is also associated with an increase in membrane resistance, and electrical polarization of the membrane indicates that the slow IPSP is nullified by a strong depolarizing current. We propose that the slow IPSP, in contrast with other types of fast IPSPs in the nervous system, is generated by an inactivation of resting sodium conductance.